Journal article
Cardiac Metabolism in Heart Failure - Implications beyond ATP production
Circulation research, Vol.113(6), pp.709-724
08/30/2013
DOI: 10.1161/CIRCRESAHA.113.300376
PMCID: PMC3896379
PMID: 23989714
Abstract
The heart has a high rate of ATP production and turnover which is required to maintain its continuous mechanical work. Perturbations in ATP generating processes may therefore affect contractile function directly. Characterizing cardiac metabolism in heart failure revealed several metabolic alterations termed metabolic remodeling, ranging from changes in substrate utilization to mitochondrial dysfunction, ultimately resulting in ATP deficiency and impaired contractility. However, ATP depletion is not the only relevant consequence of metabolic remodeling during heart failure. By providing cellular building blocks and signaling molecules, metabolic pathways control essential processes such as cell growth and regeneration. Thus, alterations in cardiac metabolism may also affect the progression to heart failure by mechanisms beyond ATP supply. Our aim is therefore to highlight that metabolic remodeling in heart failure not only results in impaired cardiac energetics, but also induces other processes implicated in the development of heart failure such as structural remodeling and oxidative stress. Accordingly, modulating cardiac metabolism in heart failure may have significant therapeutic relevance that goes beyond the energetic aspect.
Details
- Title: Subtitle
- Cardiac Metabolism in Heart Failure - Implications beyond ATP production
- Creators
- Torsten Doenst - Department of Cardiothoracic Surgery, Jena University Hospital, Friedrich-Schiller-University of Jena, 07747 Jena, GermanyT. Dung Nguyen - Department of Cardiothoracic Surgery, Jena University Hospital, Friedrich-Schiller-University of Jena, 07747 Jena, GermanyE. Dale Abel - Division of Endocrinology, Metabolism and Diabetes, and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA
- Resource Type
- Journal article
- Publication Details
- Circulation research, Vol.113(6), pp.709-724
- DOI
- 10.1161/CIRCRESAHA.113.300376
- PMID
- 23989714
- PMCID
- PMC3896379
- ISSN
- 0009-7330
- eISSN
- 1524-4571
- Grant note
- R01 HL108379 || HL / National Heart, Lung, and Blood Institute : NHLBI
- Language
- English
- Date published
- 08/30/2013
- Academic Unit
- Roy J. Carver Department of Biomedical Engineering; Fraternal Order of Eagles Diabetes Research Center; Biochemistry and Molecular Biology; Endocrinology and Metabolism; Internal Medicine
- Record Identifier
- 9984024413302771
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